A20 and ABIN-3 possibly promote regression of trehalose 6,6′-dimycolate (TDM)-induced granuloma by interacting with an NF-kappa B signaling protein, TAK-1

Sakai, Yusuke; Uchida, Kazuyuki; Nakayama, Hiroyuki

doi:10.1007/s00011-011-0406-6

Cited by 7 publications

(4 citation statements)

References 51 publications

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“…identified to be a gene whose expression is rapidly induced by tumor necrosis factors (18). The protein encoded by this gene is a zinc finger protein and it has been shown to inhibit NF-κB activation as well as TNF-mediated apoptosis (19). The anti-apoptotic protein Bcl-2 has been demonstrated to prevent disruption of mitochondrial physiology and block cytochrome c release from mitochondria, which is a response gene of p53 and involved in p53-regulated apoptosis (20,21).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen gas inhalation protects against liver ischemia/reperfusion injury by activating the NF-κB signaling pathway

Zhang

Tang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Hydrogen has been demonstrated to function as a novel antioxidant and exert therapeutic antioxidant activity in a number of diseases. The present study was designed to investigate the effect of hydrogen inhalation on liver ischemia/reperfusion (I/R) injury in rats. The portal triad to the left lobe and the left middle lobe of the liver were completely occluded for 90 min. This was followed by reperfusion for 180 min. The rats subsequently underwent syngeneic orthotopic liver transplantation. Inhalation of various concentrations (1, 2 and 3%) of hydrogen gas and its administration for different durations (1, 3 and 6 h) immediately prior to the I/R injury allowed the optimal dose and duration of administration to be determined. Liver injury was evaluated through biochemical and histopathological examinations. The expression levels of proinflammatory cytokines, including tumor necrosis factor (TNF)-α and interleukin (IL)-6, were measured by enzyme-linked immunosorbent assay and quantitative polymerase chain reaction (qPCR). Liver nuclear factor κB (NF-κB) was detected by qPCR and western blot analysis. Inhalation of hydrogen gas at 2% concentration for 1 h significantly reduced the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, the expression of cytokines, including IL-6, TNF-α, early growth response protein 1 (Egr-1) and IL-1β, and morphological damage. In addition, the mRNA and protein expression levels of NF-κB, heme oxygenase-1 (HO-1), B-cell lymphoma 2 (Bcl-2) and zinc finger protein A20 (A20) in rats where only the donors received hydrogen were significantly increased compared with those in rats where both the donor and recipient, or only the recipient received hydrogen. The results indicate that hydrogen inhalation at 2% concentration for 1 h prior to liver transplantation protected the rats from ischemia/reperfusion injury by activation of the NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Hydrogen gas inhalation protects against liver ischemia/reperfusion injury by activating the NF-κB signaling pathway

Zhang

Tang

et al. 2015

Experimental and Therapeutic Medicine

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“…For intravenous administration, indicated amounts of AG or AG water/oil/water (w/o/w) emulsion were injected intravenously. The w/o/w emulsion containing AG was prepared as described for the preparation of w/o/w emulsion containing trehalose‐6,6′‐dimycolate (TDM) in previous reports (Bekierkunst et al, 1969 ; Yarkoni & Rapp, 1977 ; Sakai et al, 2012 ). Briefly, 100 μg of chemically synthesized AG was dissolved in 3.2 μl of Freund’s incomplete adjuvant (Chemicon, Temecula, CA), and then, 3.2 μl of 0.1 M PBS was added.…”

Section: Methodsmentioning

confidence: 99%

Sensing of mycobacterial arabinogalactan by galectin‐9 exacerbates mycobacterial infection

Zheng

et al. 2021

EMBO Reports

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Mycobacterial arabinogalactan (AG) is an essential cell wall component of mycobacteria and a frequent structural and biosynthetical target for anti-tuberculosis (TB) drug development.Here, we report that mycobacterial AG is recognized by galectin-9 and exacerbates mycobacterial infection. Administration of AG-specific aptamers inhibits cellular infiltration caused by Mycobacterium tuberculosis (Mtb) or Mycobacterium bovis BCG, and moderately increases survival of Mtb-infected mice or Mycobacterium marinum-infected zebrafish. AG interacts with carbohydrate recognition domain (CRD) 2 of galectin-9 with high affinity, and galectin-9 associates with transforming growth factor b-activated kinase 1 (TAK1) via CRD2 to trigger subsequent activation of extracellular signal-regulated kinase (ERK) as well as induction of the expression of matrix metalloproteinases (MMPs). Moreover, deletion of galectin-9 or inhibition of MMPs blocks AG-induced pathological impairments in the lung, and the AG-galectin-9 axis aggravates the process of Mtb infection in mice. These results demonstrate that AG is an important virulence factor of mycobacteria and galectin-9 is a novel receptor for Mtb and other mycobacteria, paving the way for the development of novel effective TB immune modulators.

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“…10,11 In response to an external signal, the zinc finger protein A20, which is a ubiquitin editing enzyme that controls ubiquitination and deubiquitination of target proteins, binds to members of the TNIP family, including TNIP1 (TNFAIP3 interacting protein 1), TNIP2 (TNFAIP3 interacting protein 2), and TNIP3 (TNFAIP3 interacting protein 3); subsequently the complex promotes ubiquitination and proteasomal degradation of proteins such as TRAF2, RIP and NEMO, leading to phosphorylation of IκB, and as a result, suppresses NF-κB activation. 12,13 However, in breast cancers, the mechanisms that regulate the factors in the negative feedback loop of the NF-κB signaling pathway require further delineation.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-423 Promotes Breast Cancer Invasion by Activating NF-κB Signaling</p>

Dai¹,

Zhao²,

Li³

et al. 2020

OTT

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Breast cancer has become the most common malignancy among women worldwide; therefore, novel diagnostic and prognostic markers and therapeutic targets are urgently required. NF-κB signaling plays a pivotal role in enhancing breast cancer malignant phenotypes, especially cancer invasion and metastasis, which is the main cause of death in cancer patients. TNIP2, an important inhibitor of the NF-κB pathway, is known to involve a negative feedback loop of the NF-κB signaling cascade and to regulate tumor aggressiveness in various cancer types. However, the mRNA level of TNIP2 is barely altered in breast cancer; thus, the mechanism that regulates TNIP2 in breast cancer still needs to be elucidated. Methods: We analyzed the expression and prognosis of miR-423 in a TCGA BRCA miRNA cohort and in clinical specimens. We detected the invasive capacity through a Matrigel-coated Transwell penetration assay, a three-dimensional (3D) spheroid invasion assay and a wound healing assay. Then, we applied luciferase assays, real-time PCR assays and Western blotting to further study the mechanism. Results: In this study, analysis of the TCGA BRCA miRNA cohort and clinical specimens demonstrated that miR-423 was upregulated in human breast cancers and was positively correlated with clinical stage, poor overall survival and metastasis classification. Moreover, the invasiveness of breast cancer cells was enhanced by ectopic expression of miR-423 and inhibited by miR-423 downregulation. Mechanistically, upregulation of miR-423 led to activation of the NF-κB signaling pathway and elevated expression of snail and twist, while repression of miR-423 inhibited this pathway. Furthermore, the results indicated that TNIP2 is a target gene of miR-423, and suppression of TNIP2 resulted in increased invasiveness in miR-423-silenced cells. Conclusion: Our results suggest that miR-423 is a crucial factor that enhances breast cancer cell invasion through the NF-κB signaling pathway and shed light on miR-423 as a promising prognostic and therapeutic marker for metastatic breast cancer.

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A20 and ABIN-3 possibly promote regression of trehalose 6,6′-dimycolate (TDM)-induced granuloma by interacting with an NF-kappa B signaling protein, TAK-1

Abstract: The results suggest that ABIN-3 contributed to granuloma regression by interacting with TAK-1 and, as a consequence, inhibiting activation of NF-kappa B pathway.

Cited by 7 publications

References 51 publications

Hydrogen gas inhalation protects against liver ischemia/reperfusion injury by activating the NF-κB signaling pathway

Hydrogen gas inhalation protects against liver ischemia/reperfusion injury by activating the NF-κB signaling pathway

Sensing of mycobacterial arabinogalactan by galectin‐9 exacerbates mycobacterial infection

<p>miR-423 Promotes Breast Cancer Invasion by Activating NF-κB Signaling</p>

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